Linking Metabolic Dysfunction to Atherosclerosis Via Activation of Macrophage CD36 Gene Transcription by Retinol Binding Protein-4
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Article, see p 1339
Differentiation of intimal macrophages into lipid-laden foam cells is a sine qua non of atherogenesis at all stages of plaque development, but atherogenesis remains an incompletely understood process. Many factors contribute to foam cell formation within the developing atheroma, but ultimately, an imbalance between uptake of cholesterol from modified low-density lipoprotein (LDL) (eg, oxidized or aggregated LDL particles) via pattern recognition receptors of the innate immune system such as CD36 and efflux of cholesterol to high-density lipoprotein or apolipoprotein A via ABC family transporters is the driving force.
Circulating levels of retinol binding protein-4 (RBP4), a plasma retinol transporter and adipokine, were found >10 years ago1 by Barbara Kahn’s laboratory to correlate with insulin resistance, type 2 diabetes mellitus, and metabolic syndrome; subsequent studies showed associations of RBP4 with cardiovascular disease.2 The Kahn laboratory later showed that RBP4 …